In frog diluting segment transepithelial K+ net flux (JKte) occurs via trans- and paracellular transport routes. Inhibition of transcellular K+ transport discloses JKte across the shunt-pathway. By means of K+-sensitive microelectrodes we have measured secretory JKte induced by an acute K+ load, in the diluting segment of the isolated and doubly-perfused frog kidney. Transcellular K+ transport was inhibited by blocking the luminal K+ permeability either directly by barium or indirectly by the diuretic drug amiloride (via intracellular acidification induced by inhibition of Na+/H+ exchange), by the Na+/K+ pump inhibitor ouabain or by inducing an acute acid load. All experimental maneouvers led to a reduction of secretory JKte to about 50% of the control JKte. The apparent permeability coefficient for K+ of this nephron portion after inhibition of transcellular secretory JKte was reduced to a similar extent. We conclude: In frog diluting segment the ratio of trans- over paracellular JKte is close to unity. This ratio represents a minimum estimate because inhibition of the transcellular K+ pathway by barium, amiloride or an acute acid load may have been incomplete. Acidosis and/or amiloride exert large antikaliuretic effects due to the inhibition of the luminal K+ permeability.